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BCS 110 Ch. 13
Learning and Memory
Terms in this set (51)
Pairing two stimuli changes the response to one of them.
Conditioned Stimulus (CS)
First part of classical conditioning experiment, initially illicits no response of note.
Unconditioned Stimulus (UCS)
Second step in Classical Conditioning, presented after CS, elicits UCR.
Unconditioned Response (UCR)
Elicited upon exposure to the UCS.
Conditioned Response (CR)
New, learned response to the CS after exposure to pairings of the CS and UCS.
An individual's response leads to a reinforcer or punishment.
Any event that increases the future probability of the response.
An event that suppresses the frequency of the response.
Difference between Classical Conditioning and Operant Conditioning
In OC, the individual's response determines the outcome (reinforcer or punishment), whereas in CC the CS or UCS occur at certain times regardless of the individual's behavior.
Physical representation of what has been learned.
Karl Lashley's view of learning that all parts of the cortex contribute equally to complex behaviors such as learning, and any part of the cortex can substitute for any other.
Karl Lashley's view of learning that the cortex works as a whole, and more cortex is better.
Assumptions in Lashley's Conclusions
1. The cerebral cortex is the best or only place for such an engram.
2. All kinds of memory are physiologically the same.
Lateral Interpositus Nucleus (LIP)
A nucleus of the cerebellum, essential for learning and retention. Responsible for extinction of learned response. Suppression prevents learning.
Midbrain motor area that receives input from the cerebellum. Suppression prevents response, but not learning.
Differences between STM and LTM
1. Capacity. STM has ~7 spaces in lists. LTM has undefined capacity.
2. How rapidly they fade. STM will fade quickly unless rehearsed. LTM can be recalled year later.
3. Recall. Once lost, an STM is gone forever. A hint can help reconstruct a LTM.
The process of moving memories from STM to LTM.
Baddeley and Hitch's idea that memory doesn't stop at a station (STM) on its road to the LTM but is instead the way we store information while are working with it. Studies point to the prefrontal cortex. Store information by elevated calcium levels which can potentiate longer responses.
Delayed Response Task
Responding to something heard or seen in the past.
Memory loss. Damage to hippocampus and surrounding areas, medial temporal lobe.
1. Normal STM or working memory.
2. Severe anterograde amnesia for declarative memory - difficulty forming new declarative memories.
3. Severe loss of episodic memories.
4. Better implicit than explicit memory.
Epileptic patient who had his hippocampus removed. Seizures decreased, but so did his long term memory. Working memory stayed in tact. Better implicit than explicit memory.
Inability to form memories for events that happened after brain damage.
Loss of memory for events that occurred before the brain damage.
Memory of single events. Treated different from other memories. Hippocampus.
Deliberate recall of information that one recognizes as a memory.
Influence of recent experience on behavior, even if one does not recognize that influence.
The ability to state a memory in words. Hippocampus.
The development of motor skills and habits. Basal ganglia.
Delayed Matching-to-Sample Task
An animal sees an object (sample) and then, after a delay, gets a choice between two objects, from which it must choose the one that matches the sample.
Delayed Nonmatching-to-Sample Task
Same as Matching-to-Sample Task, except animal must choose the object that is different from the sample.
Maze with 8 or more arms, some of which have a bit of food or other reinforcement at the end.
Morris Water Maze Task
Maze where a rat must swim through murky water to find a rest platform that is just under the surface.
Neurotransmitters Involved in Memory
Stressful and emotional experiences increase secretion of cortisol and epinephrine(adrenaline). Small to moderate amounts of cortisol activate the amygdala and hippocampus, which enhance storage and consolidation.
Korsakoff's Syndrome (Wernicke-Korsakoff Syndrome)
Brain damage caused by prolonged thiamine deficiency. Brain area mostly affected: Dorsomedial Thalamus, main source of input for the prefrontal cortex. Apathy, confusion, and memory loss.
Common in Korsakoff's Syndrome. Patients guess to fill in memory gaps.
Better procedural than declarative memory.
Amyloid-B or B-Amyloid
Genes controlling early-onset Alzheimer's disease produce this protein that accumulates inside and outside the neurons. High levels damage axons and dendrites. These areas are called plaques.
Part of the internal support structure of the neuron. Abnormal in Alzheimer's patients. Produces tangles.
Loss of Semantic Memory. Damage in the anterior and inferior regions of the temporal lobe.
A synapse that increases in effectiveness because of simultaneous activity in the pre and post synaptic neuron.
A decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli.
An increase in response to mild stimuli as a result of exposure to more intense stimuli.
Long Term Potentiation
One or more axons connected to a dendrite bombard it with a brief but rapid series of stimuli This burst of intense stimulation leaves some of the synapses potentiated(more responsive to new input of the same type) for minutes, days or weeks.
Properties of LTP that make it a candidate for the cellular basis of learning and memory
1. Specificity-Only active cells become strengthened.
2. Cooperativity-Nearly simultaneous stimulation by 2 or more axons produces LTP much more strongly than does repeated stimulation by just one axon.
3. Associativity-Pairing a weak input with a strong input enhances later response to the weak input. Similar to Hebbian synapses.
Long Term Depression
Occurs in hippocampus and cerebellum. A prolonged decrease in response at a synapse, occurs when axons have been less active than others. Compensatory process-as one axon strengthens, one weakens.
Glutamate receptor only activated by the drug AMPA. Ionotropic-when stimulated, channels open to let Na+ in.
Glutamate receptor that can be activated by the drug NMDA. Ionotropic-when stimulated, channels open to let Na+ and Ca+ in. At rest, blocked by Magnesium ions attracted to the - charge of the cell, but can't fir through the NMDA receptors. AMPA allows in enough Na+ to positively charge the cell, expelling the Mg ion.
Protein activated when NMDA receptors open, travels to the synapse. Necessary for LTP.
Mechanisms by which LTP occurs
1. The dendrite builds more AMPA receptors or moves old ones into better position.
2. The neuron makes more NMDA receptors.
3. Dendrite makkes more branches, creating more synapses with the axon.
4. Some individual AMPA receptors become more responsive than before.
Travels from post synaptic to pre synaptic cell and modifies it.
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